Chronic intermittent hypoxia-induced neuronal apoptosis in the hippocampus is attenuated by telmisartan through suppression of iNOS/NO and inhibition of lipid peroxidation and inflammatory responses

摘要: Abstract Obstructive sleep apnea syndrome (OSAS) plays a critical role in the initiation and progression of Alzheimer׳s disease (AD), but little is known about precise mechanism OSAS-induced AD. Nitric oxide synthase (NOS) nitric (NO) are to play key roles development Several studies have confirmed that an angiotensin II type 1 receptor blocker, telmisartan, beneficially regulates NOS NO. Here, we examined neuroprotective effects telmisartan against hippocampal apoptosis induced by chronic intermittent hypoxia (CIH), most characteristic pathophysiological change OSAS. Adult male Sprague Dawley rats were subjected 8 h per day with or without for eight weeks. Neuronal CA1 region, activity, NO content, presence inflammatory agents radical oxygen species hippocampus determined. The results showed CIH activated inducible (iNOS), increased enhanced lipid peroxidation responses hippocampus. Treatment inhibited excessive iNOS generation reduced responses. In addition, significantly ameliorated CIH. conclusion, Pre-CIH administration attenuated CIH-induced partly regulating inhibiting generation, reducing